A major barrier to continued rapid progress in oculomotor neurophysiology is the inability to demonstrate connections or lack of connections between neurons that carry known oculomotor signals. Only a combination of these types of knowledge will allow us to understand how the neural circuits work. Therefore, the major goal of this research is to correlate function at the level of whole animal behavior with connectivity at the level of the single cell. The research specifically dwells on the vertical gaze system. In the clinic, impairment of vertical or horizontal gaze is equally common, but the diagnostic significance of vertical gaze disorders is less well appreciated, because the neural circuitry underlying vertical eye movements is less well understood. The proposed research is aimed directly at resolving this problem. The so called accessory oculomotor nuclei, located in the rostral brainstem near the oculomotor complex have been implicated in vertical gaze control by clinical evidence and by studies in experimental animals. In particular, neurons inthe pre-rubral field and interstitial nucleus of Cajal are thought to project directly to extraocular motoneurons subserving vertical eye movements, and to provide signals for rapid eye movements and the vertical vestibuloocular relfex respectively. In cat, the connectivity of these cells will be examined using intracellular recording, and then the axonal projection of the penetrated cell will be labeled by intracellular injection of horseradish peroxidase. These experiments will provide for the first time direct evidence for or against the presumed connections between accessory oculomotor cells and extraocular motoneurons. In the alert monkey, the signals carried by accessory oculomotor cells will be analyzed in relation to both eye and head movements. Then the connectivity of the cell will be examined using microstimulation and spike triggered cross correlation methods. Finally, hypotheses about the functions of the accessory oculomotor nuclei will be tested by selectively destroying them with the neurotoxin, kainic acid. The resultant deficit and possible recovery mechanisms will be a useful animal model for disease processes affecting these nuclei and provide valuable information to the clinician.